TY - JOUR
T1 - Anomalous growth hormone responses to thyrotropin-releasing hormone and glucose in cirrhotic patients
T2 - The effect of metergoline
AU - Salerno, F.
AU - Cocchi, D.
AU - Frigerio, C.
AU - Colombo, A. M.
AU - Müller, E. E.
PY - 1980
Y1 - 1980
N2 - The anomalous GH response to TRH or glucose loading was evaluated in patients with severe liver disease untreated or pretreated with metergoline (MCE), a potent antiserotonergic drug. In 9 patients, injection of 400 μg TRH as a bolus induced a clear-cut GH rise (>8 ng/ml), with peak levels 15-90 min post injection. Pretreatment with MCE did not modify baseline GH levels but potentiated the TRH-induced GH rise in 4 patients. In addition, 2 of 8 TRH nonresponder patients developed the anomalous GH response after MCE pretreatment. Like MCE, methysergide, another antiserotoninergic drug, potentiated the TRH-induced GH rise in 2 of 4 patients. Glucose administration (100 g, orally) induced a paradoxical rise of GH in 9 of 10 patients; after MCE, the paradoxical GH response to glucose was potentiated in 6 patients. These data provide the first experimental evidence that a derangement in brain monoamine (serotonin) function is actually involved in the occurrence of anomalous GH responses in subjects with severe liver disease.
AB - The anomalous GH response to TRH or glucose loading was evaluated in patients with severe liver disease untreated or pretreated with metergoline (MCE), a potent antiserotonergic drug. In 9 patients, injection of 400 μg TRH as a bolus induced a clear-cut GH rise (>8 ng/ml), with peak levels 15-90 min post injection. Pretreatment with MCE did not modify baseline GH levels but potentiated the TRH-induced GH rise in 4 patients. In addition, 2 of 8 TRH nonresponder patients developed the anomalous GH response after MCE pretreatment. Like MCE, methysergide, another antiserotoninergic drug, potentiated the TRH-induced GH rise in 2 of 4 patients. Glucose administration (100 g, orally) induced a paradoxical rise of GH in 9 of 10 patients; after MCE, the paradoxical GH response to glucose was potentiated in 6 patients. These data provide the first experimental evidence that a derangement in brain monoamine (serotonin) function is actually involved in the occurrence of anomalous GH responses in subjects with severe liver disease.
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M3 - Article
C2 - 6773980
AN - SCOPUS:0018945596
VL - 51
SP - 641
EP - 646
JO - Journal of Clinical Endocrinology and Metabolism
JF - Journal of Clinical Endocrinology and Metabolism
SN - 0021-972X
IS - 3
ER -